The transient receptor potential (TRPA – ankyrin) receptor has been linked to pathological conditions in cardiac function in mammals. To better understand the function of the TRPA in regulation of the heart function the Drosophila melanogaster model was used to express TRPA in heart and body wall muscles. Heartbeat of intact larvae as well as hearts in situ, devoid of hormonal and neural input indicate that strong activation of larvae over expressing TRPA at 30 or 370C stopped the heart from beating, but in a diastolic state. Cardiac function would recover upon cooling and short exposure to high temperature. Parental control lines increased heart rate transiently at 300C and 370C and, the heart rates at 370C would slow down within 3 minutes for in-situ vs in-vivo preparations. The in-situ preparations maintained an elevated rate at 30C. The heartbeat in the TRPA expressing line could not be revived at 370C with serotonin. Thus, TRPA activation may have allowed enough Ca2+ influx to activate K(Ca)+ channels into a form of diastolic stasis. TRPA activation in body wall muscle confirmed a depolarization of membrane. The Phaenicia sericata blow fly increased heartbeat at 30 and 370C and did not cease beating as compared to the Drosophila control lines. Over expressing TRPA in Drosophila and maintaining them at 370C would result in death within 24 hours whereas the blow flies thrived.